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• W2017868517 abstract "Activation of transcription in response to low oxygen tension is mediated by the hypoxia-inducible factor-1 (HIF-1). HIF-1 is a heterodimer of two proteins: aryl hydrocarbon receptor nuclear translocator and the oxygen-regulated HIF-1α. The C-terminal activation domain of HIF-1α has been shown to interact with cysteine/histidine-rich region 1 (CH1) of the coactivator CBP/p300 in a hypoxia-dependent manner. However, HIF forms lacking C-terminal activation domain (naturally occurring or genetically engineered) are still able to activate transcription of target genes in hypoxia. Here, we demonstrate that the N-terminal activation domain (N-TAD) of HIF-1α interacts with endogenous CBP and that this interaction facilitates its transactivation function. Our results show that interaction of HIF-1α N-TAD with CBP/p300 is mediated by the CH3 region of CBP known to interact with, among other factors, p53. Using fluorescence resonance energy transfer experiments, we demonstrate that N-TAD interacts with CH3 in vivo. Coimmunoprecipitation assays using endogenous proteins showed that immunoprecipitation of CBP in hypoxia results in the recovery of a larger fraction of HIF-1α than of p53. Chromatin immunoprecipitation demonstrated that at 1% O2 CBP is recruited to a HIF-1α but not to a p53 target gene. Upon activation of both pathways, lower levels of chromatin-associated CBP were detected at either target gene promoter. These results identify CBP as the coactivator directly interacting with HIF-1α N-TAD and mediating the transactivation function of this domain. Thus, we suggest that in hypoxia HIF-1α is a major CBP-interacting transcription factor that may compete with other CBP-dependent factors, including p53, for limiting amounts of this coactivator, underscoring the complexity in the regulation of gene expression by HIF-1α. Activation of transcription in response to low oxygen tension is mediated by the hypoxia-inducible factor-1 (HIF-1). HIF-1 is a heterodimer of two proteins: aryl hydrocarbon receptor nuclear translocator and the oxygen-regulated HIF-1α. The C-terminal activation domain of HIF-1α has been shown to interact with cysteine/histidine-rich region 1 (CH1) of the coactivator CBP/p300 in a hypoxia-dependent manner. However, HIF forms lacking C-terminal activation domain (naturally occurring or genetically engineered) are still able to activate transcription of target genes in hypoxia. Here, we demonstrate that the N-terminal activation domain (N-TAD) of HIF-1α interacts with endogenous CBP and that this interaction facilitates its transactivation function. Our results show that interaction of HIF-1α N-TAD with CBP/p300 is mediated by the CH3 region of CBP known to interact with, among other factors, p53. Using fluorescence resonance energy transfer experiments, we demonstrate that N-TAD interacts with CH3 in vivo. Coimmunoprecipitation assays using endogenous proteins showed that immunoprecipitation of CBP in hypoxia results in the recovery of a larger fraction of HIF-1α than of p53. Chromatin immunoprecipitation demonstrated that at 1% O2 CBP is recruited to a HIF-1α but not to a p53 target gene. Upon activation of both pathways, lower levels of chromatin-associated CBP were detected at either target gene promoter. These results identify CBP as the coactivator directly interacting with HIF-1α N-TAD and mediating the transactivation function of this domain. Thus, we suggest that in hypoxia HIF-1α is a major CBP-interacting transcription factor that may compete with other CBP-dependent factors, including p53, for limiting amounts of this coactivator, underscoring the complexity in the regulation of gene expression by HIF-1α." @default.
• W2017868517 created "2016-06-24" @default.
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• W2017868517 date "2010-01-01" @default.
• W2017868517 modified "2023-10-11" @default.
• W2017868517 title "Complex Regulation of the Transactivation Function of Hypoxia-inducible Factor-1α by Direct Interaction with Two Distinct Domains of the CREB-binding Protein/p300" @default.
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• W2017868517 doi "https://doi.org/10.1074/jbc.m109.021824" @default.
• W2017868517 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2807317" @default.
• W2017868517 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19880525" @default.
• W2017868517 hasPublicationYear "2010" @default.
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